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ESMO Investor/Analyst Event in Munich

October 21, 2018

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This presentation contains forward-looking statements, which express the current beliefs and expectations of management. Such statements are based on current expectations and involve a number of known and unknown risks and uncertainties that could cause Clovis Oncology’s future results, performance or achievements to differ significantly from the results, performance or achievements expressed or implied by such forward-looking statements. Examples of forward-looking statements discussed in this presentation include, among others, statements regarding our expectation of timing for submission and potential approval of our filings for rucaparib with the FDA and the MAA. Important factors that could cause or contribute to such differences are discussed in Clovis Oncology’s filings with the U.S. Securities and Exchange Commission. Forward-looking statements speak only as of the date on which they are made, and Clovis Oncology undertakes no obligation to update publicly or revise any forward-looking statement, whether as a result of new information, future developments or otherwise.

This presentation is being webcast and a replay will be available at clovisoncology.com

Forward-looking Statements

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Tonight’s Agenda

Time Topic Presenter

6:15 Introduction Patrick MahaffyPresident and CEO, Clovis Oncology

6:20 Prostate Cancer Overview and Clovis Prostate Development Program

Dr. Lindsey Rolfe, Clovis Oncology EVP and CMO

6:30 Review of TRITON2 dataset and other highlights

Dr. Josep PiulatsMedical Oncology, Institut Catalàd’Oncologia

6:50 Q&A Dr. Lindsey RolfeDr. Josep Piulats

7:15 Closing Comments/Adjournment Patrick Mahaffy

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Significant Unmet Need Exists in Prostate Cancer

• Second most frequently diagnosed cancer in men1

– More than 164,000 men in the U.S. diagnosed each year1

– Approximately 345,000 men in the EU diagnosed each year2

• Castration-resistant prostate cancer (CRPC) has high likelihood of developing metastases3

– The 5-year survival rate is ~29% for metastatic disease4

– mCRPC remains an incurable disease usually associated with poor prognosis5

mCRPC = metastatic castration-resistant prostate cancerSources: 1. American Cancer Society Key Statistics for Prostate Cancer www.cancer.org updated January 4, 2018 2. GLOBOCAN Cancer Fact Sheets http://globocan.iarc.fr/old/FactSheets/cancers/prostate-new.asp updated 2012 3. Hotte et al. Curr Oncol. 2010; 17(Suppl 2); S72-79 4. American Cancer Society Survival Rates for Prostate Cancer www.cancer.org updated December 18, 2017 5. Sikora-Kupis et al Journal for Clinical Studies. 2015; V7I15; 45-50

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Rucaparib has Potential Utility in Prostate Cancer

• Approximately 12% of mCRPC patients have a deleterious mutation in BRCA1 or BRCA2*

– These molecular markers may be used to select patients for treatment with a PARP inhibitor

• Preclinical and limited clinical data have shown that PARP inhibitors have anti-tumor activity in HRR-deficient prostate cancer**

*Sources: Bancroft et al. Eur Urol. 2014; 66(3):489-99; Castro et al. J Clin Oncol. 2013;31(14):1748-57; Abida et al. JCO Precis Oncol. 2017;1:1-16. **Sources: Nguyen et al. Cancer Res. 2017;77(13 suppl):abstr 2476; Mateo et al. N Engl J Med. 2015;373:1697-708, Kaufman B, et al., J Clin Oncol 2015;33(3):244-50.

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Rubraca Granted Breakthrough Therapy Designation for Advanced Prostate Cancer

• FDA granted Breakthrough Therapy designation (BTD) for

Rubraca on October 2, 2018– As monotherapy treatment of adult patients with BRCA1/2-

mutated mCRPC who have received at least one prior AR-

directed therapy and taxane-based chemotherapy

– TRITON2 dataset presented at ESMO served as basis for BTD

– This is the second BTD granted for Rubraca

*, AR = androgen-receptor.

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TRITON2 in Prostate Cancer: Later Line Study for Potential Accelerated Approval

TRITON2: A Phase 2 single-arm study Initiated Q4 2016

• Enrolling patients with germline or somatic BRCA mutations as well as other deleterious mutations in other HR repair genes

• All patients will have progressed after receiving one line of taxane-based chemo and one or two lines of AR-targeted therapy in the castration-resistant setting

• Primary endpoints are confirmed radiologic ORR per modified RECIST/PCWG3 in patients with measurable disease and PSA response rate in patients without measurable disease

• Initial presentation of data at ESMO 2018

HR = homologous recombination, AR = androgen receptor, PSA = prostate-specific antigen

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TRITON3 in Prostate Cancer: Earlier Line Comparative Study for Potential Full Approval

TRITON3: A Phase 3 comparative study Initiated Q1 2017

• Enrolling patients with germline or somatic BRCA mutations and ATM mutations who have progressed on AR-targeted therapy and who have not yet received chemo in the castration-resistant setting

• The study will compare rucaparib to physician’s choice of AR-targeted therapy or chemotherapy in these patients

• Planned primary endpoint is radiologic PFS

• Study could potentially serve as confirmatory should TRITON2 study data support an accelerated approval

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9KD Study: Rubraca and Opdivo Combo in mCRPC

Phase 2 in metastatic castration-resistant prostate cancer (mCRPC)

Initiated Q4 2017

• 3 arm trial - Opdivo and Rubraca, Opdivo + docetaxel + prednisone, Opdivo + enzalutamide

• Objective to determine whether the combination meaningfully affects response rate and changes in PSA

• Mandatory tumor tissue to enable biomarker evaluation

• BMS sponsoring, conducting and funding study

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• Medical Oncologist at Institut Català d’Oncologia (ICO) since 2003

– In charge of prostate cancer, gynaecological tumors and

melanoma

• Member of Barcelona Medical College since 1998

• Licensed in Medicine and Surgery since 1998

• Received Doctorate degree in 2010– Post doctoral stay in biochemistry department at the Osaka

Medical Cancer Center 2011-2014

Introduction: Josep M. Piulats, MD, PhD

Highlights of TRITON Poster Presentations at ESMO

Josep M. Piulats, MD, PhD, Medical Oncology Unit at the Institut Catalàd’Oncologia (ICO) in Barcelona, Spain and Investigator for TRITON2 and TRITON3 studies

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Genomic Profiling of Circulating Tumour DNA (ctDNA) and Tumour Tissue for the Evaluation of Rucaparib in Metastatic Castration-Resistant Prostate Cancer (mCRPC)

Simon Chowdhury,1 Ray McDermott,2 Josep Maria Piulats,3 Jeremy D. Shapiro,4 Inge Mejlholm,5David Morris,6 Peter Ostler,7 Arif Hussain,8 Igor Dumbadze,9 Evan R. Goldfischer,10 Elias Pintus,11

Ali Benjelloun,12 Mitchell E. Gross,13 Sheela Tejwani,14 Gurkamal Chatta,15 Albert Font,16

Andrea Loehr,17 Andrew D. Simmons,17 Simon P. Watkins,17 Wassim Abida18

1Guy's Hospital and Sarah Cannon Research Institute, London, UK; 2Adelaide and Meath Hospital (Incorporating the National Children's Hospital), Dublin, UK; 3Instituto Catalan de Oncologia, Barcelona, Spain; 4Cabrini Hospital, Malvern, VIC, Australia;5Vejle Sygehus, Vejle, Denmark; 6Urology Associates Clinical Research, Nashville, TN, USA; 7Mount Vernon Cancer Centre, Northwood, UK; 8University of Maryland Greenebaum Cancer Center, Baltimore, MD, USA; 9The Urology Group, Cincinnati, OH, USA; 10Premier Medical Group of the Hudson Valley, Poughkeepsie, NY, USA; 11Frimley Health NHS Foundation Trust, Slough, UK; 12Centre Hospitalier Universitaire Dr-Georges-L.-Dumont, Moncton, NB, Canada; 13University of Southern California, Los Angeles, CA, USA; 14Henry Ford Health System, Detroit, MI, USA; 15Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA; 16Hospital Universitari Germans Trias i Pujol, Badalona, Spain; 17Clovis Oncology, Inc., Boulder, CO, USA; 18Memorial Sloan Kettering Cancer Center, New York, NY, USA

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Genomic Profiling in the TRITON Studies: Methods

• Obtaining tissue samples from prostate cancer patients can be challenging for patients and physicians

• TRITON2/3 identifies patients using plasma and/or tissue testing

• Specimens from 1516 patients, including 1311 tumor and 638 plasma, analyzed as of July 2, 2018 for TRITON2/3 during screening

• Cell-free circulating tumor DNA (cfDNA) from plasma sequenced by Foundation Medicine, Inc. (FMI) using NGS assay1 to identify deleterious germline/somatic alterations in BRCA1, BRCA2, ATM or 3 other HRR genes (CDK12, CHEK2, PALB2)

• Archival and contemporaneous tissue samples sequenced by FMI2 to identify deleterious germline/somatic alterations in BRCA1, BRCA2, ATM, or 12 other HRR genes

HRR, homologous recombination repair.; NGS = next-generation sequencing1. Clark et al. J Mol Diagn. 2018;20:686-702. 2. Frampton et al. Nat Biotechnol. 2013;31:1023-31.

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Tumor Tissue Characteristics

• Tumor tissue testing is validated to detect copy number events including homozygous loss and mutation zygosity

• 1311 archival or recent tissue samples from 1214 patients were submitted, most (88%) with a Gleason score ≥8

• The majority (84%) of samples were core needle biopsies or resections of primary prostate tumors

• The median sample age was 2.8 years (range, 4 days to 21 years)

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Tumor Tissue Screening Results

• NGS test failure rate 32%, most commonly due to insufficient tumor content or DNA yield

• NGS success rate higher for metastatic samples (74%) than for primary prostate tumor tissue (56%)

• Observed BRCA1/2 alteration frequency in tissue was higher in later line TRITON2 patients (10.5%) than in less advanced TRITON3 patients (6.5%)

• Consistent with the patient populations enrolled, the percentage of patients with AR amplification was higher in TRITON2 as compared to TRITON3

AR, androgen receptor; HRR, homologous recombination repair; NGS, next-generation sequencing.

Alteration

Frequency in tissueTRITON2 (n=487)

TRITON3(n=385)

BRCA1 alteration 1.8% 1.3%

BRCA2 alteration 8.6% 5.5%

ATM alteration 6.6% 5.7%

CDK12 alteration 6.8% 5.4%

TP53 alteration 38.4% 37.1%

AR amplification 9.9% 4.7%

PTEN loss 25.4% 19.5%

ERG-TMPRSS2fusion 28.3% 28.1%

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Plasma cfDNA Characteristics

• Plasma samples are easily obtained and generally contain sufficient cfDNA for NGS processing, but assay is not validated to measure TMB or homozygous loss

• 638 plasma samples from 606 patients progressing on prior therapy were submitted for screening

• The median age of plasma samples was 2 days (range, 1 to 10 days)

• 620 (97%) samples had sufficient cfDNA for successful NGS

cfDNA, cell-free circulating tumour DNA; mCRPC, metastatic castration-resistant prostate cancer; NGS, next-generation sequencing; TMB, tumour mutational burden.

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Plasma cfDNA Results

• The BRCA1/2 alteration frequency was 8.0% in the earlier line TRITON3 patients, compared to 11.7% in the more advanced TRITON2 patients

– This frequency excludes homozygous loss of BRCA1/2, which the assay is not validated to detect

• The BRCA1/2 alteration frequencies in TRITON2 and TRITON3 were higher in plasma samples than in tissue samples– Most tissue samples were archival and

may be less representative of the metastatic disease state, which has been reported to have an increased frequency of BRCA1/2 alterations1

• The alteration frequencies in ATM, CDK12, and TP53 were also lower in TRITON3 than in TRITON2

1. Abida et al. JCO Precis Oncol. 2017;1:1-16.

Alteration

Frequency in plasmaTRITON2 (n=343)*

TRITON3(n=263)*

BRCA1 alteration 2.3% 1.9%

BRCA2 alteration 9.6% 6.8%

ATM alteration 14.6% 8.2%

CDK12 alteration 6.1% 3.1%

TP53 alteration 48.1% 44.9%

*For ATM and CDK12 n=246 for TRITON2 and n=194 for TRITON3.

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BRCA1/2 Concordance Between Tissue and Plasma

• Concordance between BRCA1/2 mutations in tissue and plasma evaluated in 161 patients with both tissue and plasma samples, 34 with a BRCA1/2mutation

• Median time between tissue and plasma sample collection 2.5 years (range, 4 days to 21 years), with 19% (31/161) tissue and plasma samples collected within a 30 day window

• 74% (25/34) patients with BRCA1/2 mutation identified by both tissue and plasma sample

N=161 sample pairs

PlasmaBRCA1/2+

PlasmaBRCA1/2-

TissueBRCA1/2+

25/34(74%)

4/34(12%)

Tissue BRCA1/2-

5/34(15%)

127/161(79%)

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High Concordance between Plasma and Tissue; Plasma Testing Preferred

• TRITON2 and TRITON3 studies of Rubraca are enrolling mCRPC patients with HRR gene alterations

• Tumor tissue and plasma assays successfully identify patients with HRR gene alteration

– High concordance between alterations detected in the tissue and plasma assays

– Tumor tissue testing measures TMB copy number events, but higher test failure rate than plasma

– Suitable tumor tissue is not always accessible in advanced prostate cancer

– cfDNA plasma sample testing is less invasive and more sensitive than tissue testing and has a low testing failure rate (3%), but is not validated to detect all copy number events

• Overall, plasma testing more suitable for prostate cancer testing than tumor

cfDNA, cell-free circulating tumour DNA; HRR, homologous recombination repair; mCRPC, metastatic castration-resistant prostate cancer; NGS, next-generation sequencing; PARP, poly(ADP-ribose) polymerase; TMB, tumourmutational burden.1. Abida et al. ESMO 2018 793PD.

Q&A

Replay will be available at www.clovisoncology.com

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Preliminary Results from TRITON2: A Phase 2 Study of Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Associated with Homologous Recombination Repair (HRR) Gene Alterations

Wassim Abida,1 Alan H. Bryce,2 Nicholas J. Vogelzang,3 Robert J. Amato,4 Ivor Percent,5Jeremy Shapiro,6 Ray McDermott,7 Arif Hussain,8 Akash Patnaik,9 Daniel Petrylak,10

Charles J. Ryan,11 Thomas Stanton,12 Jingsong Zhang,13 Andrew D. Simmons,14

Darrin Despain,14 Melanie Collins,14 Tony Golsorkhi,14 Howard I. Scher,1 Simon Chowdhury15

1Memorial Sloan Kettering Cancer Center, New York, NY, USA; 2Mayo Clinic, Phoenix, AZ, USA; 3Comprehensive Cancer Centers of Nevada, Las Vegas, NV, USA; 4Science Center, Houston, TX, USA; 5Florida Cancer Specialists, Port Charlotte, FL, USA; 6Cabrini Hospital, Malvern, VIC, Australia; 7Adelaide and Meath Hospital (Incorporating the National Children's Hospital), Dublin, Ireland; 8University of Maryland Greenebaum Cancer Center, Baltimore, MD, USA; 9University of Chicago Comprehensive Cancer Center, Chicago, IL, USA; 10Yale University, Yale Cancer Center, New Haven, CT, USA; 11University of Minnesota, Minneapolis, MN, USA; 12St. Joseph Health Cancer Center, Santa Rosa, CA, USA; 13H. Lee Moffitt Cancer Center, Tampa, FL, USA;14Clovis Oncology, Inc., Boulder, CO, USA; 15Guy's Hospital and Sarah Cannon Research Institute, London, UK

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Introduction

• Limited treatment options exist for patients with mCRPC following AR–directed

therapy and taxane chemotherapy1,2

• In metastatic prostate cancer, up to 25% of patients harbor a deleterious

germline and/or somatic alteration in BRCA1, BRCA2, ATM, or other HRR

gene3-5

• In cells with HRR deficiency, inhibition of poly(ADP-ribose) polymerase (PARP)

results in cell death via synthetic lethality6-8

• Preclinical and limited clinical data have shown that PARP inhibitors have

antitumor activity in HRR-deficient prostate cancer9,10

– In preclinical studies, rucaparib demonstrated activity in prostate cancer cell lines

with reduced levels of BRCA1, BRCA2, or ATM9

HRR, homologous recombination repair; mCRPC, metastatic castration-resistant prostate cancer.NCCN Clinical Practice Guidelines in Oncology.

https://www.nccn.org/professionals/physician_gls/pdf/prostate.pdf. Accessed 21 September 2018; 3. Robinson et al. Cell. 2015;161:1215-28; 4. Pritchard et al. N Engl J Med. 2016;375:443-53; 5. Abida et al. JCO Precis Oncol. 2017;1:1-16; 6. O'Connor. Mol Cell. 2015;60:547-60; 7. Lee et al. Ann Oncol. 2014;25:32-40; 8. Scott et al. J Clin Oncol. 2015;33:1397-406; 9.

1. Parker et al. Ann Oncol. 2015;26:v69-77; 2.

Nguyen et al. Cancer Res. 2017;77(13 suppl):abstr2476; 10. Mateo et al. N Engl J Med. 2015;373:1697-708, Kaufman B, et al., J Clin Oncol 2015;33(3):244-50.

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TRITON2: Trial Design and Schema

• Eligible patients were screened for the presence of a deleterious germline or somatic alteration in BRCA1, BRCA2, ATM, or other prespecified HRR gene1

• Enrolled patients received oral rucaparib 600 mg twice daily (BID)

Treatment28-day cycles

Rucaparib 600 mg BID

Treatment until radiographic progression or discontinuation

for other reason

Screening

Identification of a deleterious somatic or germline alteration

in HRR gene*

HRR genes

BRCA1BRCA2

ATM

BARD1BRIP1CDK12CHEK2FANCA

NBN

PALB2RAD51

RAD51BRAD51CRAD51DRAD54L

• Tumor assessments Q8W for 24 weeks, then Q12W

• PSA assessments Q4W

• Patients with measurable disease at baseline: confirmed ORR per modified RECIST‡/PCWG3 by central assessment

• Patients with no measurable disease at baseline: confirmed PSA response (≥50% decrease) rate§

Primary endpoints†Key eligibility criteria

• mCRPC• Deleterious somatic or germline alteration in HRR gene

• Disease progression on AR-directed therapy (eg, abiraterone, enzalutamide, or apalutamide) for PC and 1 prior taxane-based chemotherapy for CRPC

• ECOG PS 0 or 1• No prior PARP inhibitor, mitoxantrone, cyclophosphamide, or platinum-based chemotherapy

*RECIST modified to include up to 10 target lesions, maximum 5 per site, not including prostatic bed or bone lesions; MRI allowed.

§

AR, androgen receptor; BID, twice daily; ECOG PS, Eastern Cooperative Oncology Group Performance Status; HRR, homologous recombination repair; MRI, magnetic resonance imaging; ORR, objective response rate;

PC, prostate cancer; PCWG3, Prostate Cancer Clinical Trials Working Group 3; PSA, prostate-specific antigen; Q4W, every 4 weeks; Q8W, every 8 weeks; Q12W, every 12 weeks;

Alterations detected by local testing or central testing of blood or tumour samples. †Efficacy analyses in TRITON2 will be conducted separately based on HRR gene with alteration and presence/absence of measurable disease. ‡The proportion of patients with a ≥50% decrease from baseline confirmed by a second consecutive measurement; PSA measurements performed by local laboratory.

CRPC, castration-resistant prostate cancer;mCRPC, metastatic CRPC; PARP, poly(ADP-ribose)

polymerase; PC, prostate cancer; RECIST, Response Evaluation Criteria In Solid Tumors v1.1

1. Chowdhury et al. ESMO 2018. Abst 795PD.

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Efficacy Populations

• Enrollment is ongoing in TRITON2 • As of 16 April 2018, 85 patients were enrolled in TRITON2

– At the visit cutoff date (29 June 2018), median duration of follow-up was 5.7 months (range, 2.6–16.4 months)

PSA response evaluable population

Radiographic response evaluable population

Patients enrolled* (N=85)

Patients with measurable disease and ≥16 weeks of follow-up or who discontinued treatment for any reason (n=46)

HRR gene with alterationBRCA1/2 n=25ATM n=5CDK12 n=8Other n=8

Patients with ≥8 weeks of follow-up or who discontinued treatment for any reason (n=85)

HRR gene with alterationBRCA1/2 n=45ATM n=18CDK12 n=13Other n=9

*Enrolment cutoff date: 16 April 2018. HRR, homologous recombination repair; PSA, prostate-specific antigen.

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Baseline Demographics

Characteristic

By HRR Gene with AlterationOverall(N=85)

BRCA1/2(n=45)

ATM(n=18)

CDK12(n=13)

Other*(n=9)

Age, median (range), y 71 (50–88) 72.5 (62–84) 64 (49–79) 72 (60–86) 71 (49–88)

Race, n (%)

White 35 (77.8%) 12 (66.7%) 6 (46.2%) 5 (55.6%) 58 (68.2%)

Black or African American 4 (8.9%) 3 (16.7%) 1 (7.7%) 1 (11.1%) 9 (10.6%)

Unknown 6 (13.3%) 3 (16.7%) 6 (46.2%) 3 (33.3%) 18 (21.2%)

ECOG PS, n (%)

0 16 (35.6%) 10 (55.6%) 6 (46.2%) 1 (11.1%) 33 (38.8%)

1 28 (62.2%) 8 (44.4%) 7 (53.8%) 7 (77.8%) 50 (58.8%)

≥2 1 (2.2%) 0 0 1 (11.1%) 2 (2.4%)

Baseline PSA, median (range), ng/mL 52.0(3.5–4782.0)

59.3(9.2–4350.0)

57.7(23.3–2966.5)

54.0(8.8–798.8)

54.0(3.5–4782.0)

Gleason score ≥8, n (%) 33 (73.3%) 6 (33.3%) 13 (100%) 6 (66.7%) 58 (68.2%)

Visit cutoff date: 29 June 2018.*Includes 2 patients with an alteration in FANCA, and 1 patient each with an alteration in BRIP1, CHEK2, NBN, PALB2, RAD51, BRIP1/CHEK2, or CHEK2/CDK12.ECOG PS, Eastern Cooperative Oncology Group Performance Status; HRR, homologous recombination repair; PSA, prostate-specific antigen.

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Baseline Demographics

Characteristic

By HRR Gene with AlterationOverall(N=85)

BRCA1/2(n=45)

ATM(n=18)

CDK12(n=13)

Other*(n=9)

No. prior CRPC therapies, median (range)† 2 (2–7)‡ 3 (2–6) 3 (2–4) 2 (2–4) 2 (2–7)‡

Prior therapies, n (%)§

Abiraterone 25 (55.6%) 16 (88.9%) 9 (69.2%) 8 (88.9%) 58 (68.2%)

Enzalutamide 33 (73.3%) 14 (77.8%) 12 (92.3%) 4 (44.4%) 63 (74.1%)

Abiraterone and enzalutamide 14 (31.1%) 12 (66.7%) 8 (61.5%) 3 (33.3%) 37 (43.5%)

Docetaxel 43 (95.6%) 17 (94.4%) 11 (84.6%) 8 (88.9%) 79 (92.9%)

Cabazitaxel 4 (8.9%) 4 (22.2%) 2 (15.4%) 1 (11.1%) 11 (12.9%)

Sipuleucel-T 6 (13.3%) 4 (22.2%) 1 (7.7%) 0 11 (12.9%)

Radium 5 (11.1%) 4 (22.2%) 0 1 (11.1%) 10 (11.8%)

Metastases, n (%)§

Bone 40 (88.9%) 17 (94.4%) 10 (76.9%) 7 (77.8%) 74 (87.1%)

Nodal 28 (62.2%) 5 (27.8%) 11 (84.6%) 8 (88.9%) 52 (61.2%)

Visceral 19 (42.2%) 4 (22.2%) 4 (30.8%) 1 (11.1%) 28 (32.9%)

Hepatic 8 (17.8%) 2 (11.1%) 1 (7.7%) 1 (11.1%) 12 (14.1%)

Visit cutoff date: 29 June 2018. *Includes 2 patients with an alteration in FANCA, and 1 patient each with an alteration in BRIP1, CHEK2, NBN, PALB2, RAD51, BRIP1/CHEK2, or CHEK2/CDK12. †Does not include luteinizing hormone-releasing hormone analogues, first-generation antiandrogens, hormones, corticosteroids, bone-targeted agents, hematopoietic growth factors, or docetaxel given for hormone-sensitive disease. ‡Data unavailable for 1 patient. §Categories are not mutually exclusive.CRPC, castration-resistant prostate cancer; HRR, homologous recombination repair.

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Baseline Demographics

Characteristic

By HRR Gene with AlterationOverall(N=85)

BRCA1/2(n=45)

ATM(n=18)

CDK12(n=13)

Other*(n=9)

Measurable disease at baseline (per investigator), n (%)

Yes 27 (60.0%) 5 (27.8%) 8 (61.5%) 8 (88.9%) 48 (56.5%)

No 18 (40.0%) 13 (72.2%) 5 (38.5%) 1 (11.1%) 37 (43.5%)

Gene alteration status, n (%)

Germline 15 (33.3%) 5 (27.8%) 0 0 20 (23.5%)

Somatic 30 (66.7%) 10 (55.6%) 0 0 40 (47.1%)

Not available 0 3 (16.7%) 13 (100%) 9 (100%) 25 (29.4%)

Visit cutoff date: 29 June 2018. *Includes 2 patients with an alteration in FANCA, and 1 patient each with an alteration in BRIP1, CHEK2, NBN, PALB2, RAD51, BRIP1/CHEK2, or CHEK2/CDK12. HRR, homologous recombination repair.

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Confirmed Investigator-Assessed ORR in Evaluable Patients with Measurable Disease at Baseline

• Of patients with a BRCA1/2 alteration and measurable disease at baseline, 44.0% (11/25) had a confirmed objective response by investigator assessment

Characteristic

By HRR Gene with Alteration

BRCA1/2(n=25)

ATM(n=5)

CDK12(n=8)

Other(n=8)

ORR*, n (%) [95% CI] 11 (44.0%)[24.4–65.1]

0 (0%)[0.0–52.2]

0 (0%)[0.0–36.9]

2 (25.0%)[3.2–65.1]

Complete response, n (%) 0 (0%) 0 (0%) 0 (0%) 0 (0%)

Partial response, n (%) 11 (44.0%) 0 (0%) 0 (0%) 2 (25.0%)†

Stable disease, n (%) 9 (36.0%) 4 (80.0%) 5 (62.5%) 5 (62.5%)

Progressive disease, n (%) 4 (16.0%) 1 (20.0%) 2 (25%) 1 (12.5%)

Not evaluable, n (%) 1 (4.0%) 0 1 (12.5%) 0

Visit cutoff date: 29 June 2018. Includes patients who had measurable disease at baseline per the investigator and ≥16 weeks of follow-up or who discontinued treatment.*Per modified RECIST/PCWG3 criteria. †One patient had a BRIP1 alteration and 1 patient had a FANCA alteration.CI, confidence interval; HRR, homologous recombination repair; ORR, objective response rate; PCWG3, Prostate Cancer Clinical Trials Working Group 3; RECIST, Response Evaluation Criteria In Solid Tumors v1.1.

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Best Change from Baseline in Sum of Target Lesions (n=46)

Visit cutoff date: 29 June 2018.Includes patients with measurable disease at baseline and ≥1 postbaseline scan. Each bar represents a single patient; patients with no change from baseline are shown as 0.5% for visual clarity; the lower dotted line indicates the threshold for partial response (30% decrease from baseline). HRR, homologous recombination repair; PCWG3, Prostate Cancer Clinical Trials Working Group 3; RECIST, Response Evaluation Criteria In Solid Tumors v1.1.

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Treatment Duration and Duration of Radiographic Response in Patients with a BRCA1/2 Alteration and Measurable Disease at Baseline (n=27)

Visit cutoff date: 29 June 2018. Values shown represent duration of confirmed response; onoing responses are ndicated with a +. Each bar represents time on treatment for 1 patient; ongoing radiographic responses are displayed to the visit cutoff date.

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Treatment Duration in Patients with an ATM Alteration (n=18)

Visit cutoff date: 29 June 2018. Each bar represents time on treatment for 1 patient.

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Confirmed PSA Response Rates

• Among patients with a BRCA1/2 alteration, 51.1% (23/45) had a confirmed PSA response

By HRR Gene with Alteration, n/N (%) [95% CI]

PSA Response Rate BRCA1/2 ATM CDK12 Other

All evaluable patients 23/45 (51.1%)[35.8–66.3]

0/18 (0%)[0.0–18.5]

1/13 (7.7%)*[0.2–36.0]

2/9 (22.2%)†

[2.8-60.0]

With measurable disease 17/27 (63.0%)[42.4–80.6]

0/5 (0%)[0.0–52.2]

1/8 (12.5%)*[0.3–52.7]

2/8 (25.0%)†

[3.2–65.1]

With no measurable disease 6/18 (33.3%)[13.3–59.0]

0/13 (0%)[0.0–24.7]

0/5 (0%)[0.0–52.2]

0/1 (0%)[0.0–97.5]

Visit cutoff date: 29 June 2018. Includes patients who had ≥8 weeks follow-up or who discontinued treatment.*This patient did not demonstrate an objective radiographic response. †One patient with a BRIP1 alteration and 1 patient with a FANCA alteration; both patients demonstrated a confirmed objective radiographic response.CI, confidence interval; HRR, homologous recombination repair; PSA, prostate-specific antigen.

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Best Change from Baseline in PSA (n=84)

• Enrolment of patients with a CDK12 alteration has been halted per protocol based on the lack of responses observed in these patients to date

Visit cutoff date: 29 June 2018. Includes all patients with ≥1 postbaseline PSA measurement. Each bar represents a single patient; patients with no change from baseline are shown as 0.5% for visual clarity; the upper dotted line indicates a 50% decrease from baseline PSA and the lower dotted line indicates a 90% decrease from baseline PSA. PSA increases for the 3 leftmost patients were 231%, 183%, and 126%; bars were capped at 100% for visual clarity.HRR, homologous recombination repair; PSA, prostate-specific antigen.

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Treatment Duration and Summary of TEAEs

• In the safety population (defined as all patients who received ≥1 dose of rucaparib; N=85), median treatment duration in the overall population was 3.7 months (range, 0.5–12.9 months)

– Median treatment duration in patients with a BRCA1/2 alteration was 4.4 months (range, 0.5–12.0 months)

Overall Safety Population (N=85)n (%)

At least 1 TEAE 81 (95.3%)

At least 1 TEAE grade ≥3 45 (52.9%)

Treatment interruption and/or dose reduction due to TEAE 45 (52.9%)

Treatment interruption due to TEAE 41 (48.2%)

Dose reduction due to TEAE 25 (29.4%)*

TEAE leading to discontinuation 5 (5.9%)†

Death due to TEAE 1 (1.2%)‡

Visit cutoff date: 29 June 2018.

One patient each (1.2%) discontinued due to anaemia/decreased haemoglobin, asthenia/fatigue, decreased appetite, and general physical health deterioration; 1 patient (1.2%) discontinued due to TEAEs of asthenia/fatigue, decreased appetite, and weight loss.

*The most common were asthenia/fatigue (8.2%), anaemia/decreased haemoglobin (7.1%), thrombocytopenia/decreased platelet count (5.9%), and nausea (4.7%). †

‡Due to disease progression. TEAE, treatment-emergent adverse event.

35

Most Common (≥10%) TEAEs of Any Grade in All Patients Regardless of Causality

Overall Safety Population (N=85)Any Grade,

n (%)Grade ≥3,

n (%)Asthenia/fatigue 38 (44.7%) 4 (4.7%)Nausea 36 (42.4%) 3 (3.5%)Anaemia/decreased haemoglobin 24 (28.2%) 13 (15.3%)Decreased appetite 24 (28.2%) 3 (3.5%)Constipation 19 (22.4%) 1 (1.2%)ALT/AST increased 18 (21.2%) 4 (4.7%)Vomiting 17 (20.0%) 0Diarrhoea 16 (18.8%) 1 (1.2%)Arthralgia 11 (12.9%) 1 (1.2%)Dizziness 11 (12.9%) 0Back pain 10 (11.8%) 2 (2.4%)Oedema peripheral 10 (11.8%) 0Weight decreased 10 (11.8%) 0Dysgeusia 9 (10.6%) 0Dyspnoea 9 (10.6%) 0Haematuria 9 (10.6%) 3 (3.5%)

Visit cutoff date: 29 June 2018.. ALT, alanine aminotransferase; AST, aspartate aminotransferase; TEAE, treatment-emergent adverse event.

36

Summary

• Rubraca has encouraging antitumor activity in patients with a deleterious alteration in BRCA1 or BRCA2

– Among evaluable patients with a BRCA1/2 alteration, 44.0% (11/25) had a confirmed radiographic response and 51.1% (23/45) had a confirmed PSA response

• Confirmed radiographic responses have not yet been observed in patients with ATM or CDK12 gene alterations

– Some reductions in target lesion diameters and PSA measurements have been observed in these patients

• Preliminary safety for Rubraca in men with mCRPC are consistent with those observed in patients with ovarian cancer and other solid tumors1–5

• Enrollment in TRITON2 is ongoing• Breakthrough Therapy designation granted October 2 for Rubraca for the

treatment of patients with BRCA1/2-mutated mCRPC• Supplemental NDA planned by end of 2019

1. Kristeleit et al. Clin Cancer Res. 2017;23:4095-106; 2. Swisher et al. Lancet Oncol. 2017;18:75-87; 3. Coleman et al. Lancet. 2017;390:1949-61; .4.Rubraca (rucaparib) tablets [prescribing information]. Boulder, CO: Clovis Oncology, Inc.; 2018; 5. Rubraca (rucaparib) tablets [summary of product characteristics]. Boulder, CO: Clovis Oncology, Inc.; 2018.

Q&A

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